Bisphenol A (BP-A, 4,4' Isopropylidenediphenol) is one of the key ingredients or precursor materials for polycarbonate plastic and epoxy resinproduction. Animals and humans can be exposed to this xenobiotic substance because BPA is found in the linings of food/beverage cans and can leak into food items. After ingestion andabsorption of a xenobiotic from the gastrointestinal tract, the liver is the primary organ associated with the metabolism of xenobiotics.  In the adult liver, Cytochrome P-450-dependent monooxygenases play a two-fold role in xenobiotic metabolism associated with the elimination of xenobiotics and the formation of bioactive or toxic metabolites.Hepatic xenobiotic metabolism is influenced by the animal strain, species, sex, age, diurnal rhythm, and effects of enzyme inducers/inhibitors.Of concern are observations indicating that premature infants possess a significant content of the industrial chemical and putative endocrine disruptor BPA that is ten-fold greater than in adults. There is evidence that BPA is metabolized by several UDP-glucuronosyltransferases Also, the early postnatal period is sensitive to exposure effects of xenobiotics, which can impair hepatic function and result in morbidity and mortality. However, the developmental effectsof BPA on oxidative stress, apoptosis, inflammation, and mitochondria in the liver have received only a little attention.  Hence, this study was performed to investigate the BPA effects on prooxidant, antioxidant, proapoptotic, and pro-inflammatory markers in the liver of growing rats.  BPAwas fed to 21-day-old male Long-Evans rats in drinking water (5 micrograms/L) for 14 days.  Since BPA was dissolved in DMSO (0.001%), control animals were provided with watercontaining 0.001% DMSO for 14 days.  Control and BPA-treated animals were sacrificed on day 35 postpartum. Liver tissues were obtained from all experimental groups to analyze oxidative stress (Reactive Oxygen Species, Nitrite, Glutathione, and Lipid Peroxide Content), inflammation (Interleukin Converting Enzyme-1 (ICE-1) activity), apoptosis (caspase-3 activity) and mitochondrial function (NADH content). Statistical analysis was performed using Prism-V software in addition to in-silico analyses with the SwissADME software to determine the physicochemical properties of BPA.  BPA had no significant effect on the markers of apoptosis, inflammation, and mitochondrial function but depleted hepatic glutathione content (P<0.05).  In-silico analysis indicated that BPA can be effectively absorbed in the gastrointestinal tract. Furthermore, BPA is not an inhibitor of p-Glycoprotein but suppressed CYP1A2, CYP2C19, and CYP2C9 activity. Although additional studies are warranted, the present results showed that short-term exposures to BPA caused prooxidant depletion and suppressed hepatic enzyme activity without affecting apoptosis and inflammation.